Pyloric Stenosis

Pylorus is the name of the outflow tract of the stomach, the muscle in the wall controls how quickly the stomach empties.

For some reason, this muscle can become hypertrophied in the first month or two of life, to the point that the baby begins to vomit with feeds, become dehydrated and lose weight. Remains hungry of course, which may not be the case with some of the differentials.

The vomit is non-bilious of course, as the obstruction is above the bile duct.

4 male:1 female. Less common in black/Asian groups. Maternal history is more significant than paternal! NB Associated with TOF, other abnormalities. Associated with erythromycin use in infancy, particularly in first 14 days of life.

1st week to 5 months, but usually after 3 weeks. Only 6% present within 14 days of life – increasing proportion over time? (Even before US available) More likely to have family history?

Preterm babies make up only 3% of cases, and symptoms/signs tend to be less dramatic. Unclear whether USS criteria (below) are valid for preterms. [Arch Peds Adol Med 1996]


Peristalsis may be visible through abdominal wall. Olive shaped mass (2 cm diameter) felt RUQ just lateral to midline, under liver (sit on left side), after vomit.

When well established vomiting, hypochloraemic, hypokalaemic alkalosis characteristic (but not 100% specific).

On ultrasound scan, muscle thickness more than 3mm, transverse pyloric diameter more than 14mm (length similarly) – ie 3.14 (Pi, the mathematical constant)! [radiopaedia]

Differential diagnosis = reflux, sepsis, cow’s milk intolerance, other surgical condition eg malrotation, raised intracranial pressure, Congenital Adrenal Hyperplasia, biochemical imbalance eg renal tubular acidosis, inborn error of metabolism etc.


Surgical pyloromyotomy (Ramstedt’s)- usually laparascopic. Quite a minor procedure, since the muscle is incised and then left to heal without any need to enter bowel itself or repair anything.